This presentation briefly discusses the approach to a child presenting with acute flaccid paralysis including a history and examination based distinction between its various etiologies and a summary on the diagnostic approach to such cases and their management with a brief mention on AFP surveillance.

1. Acute Flaccid Paralysis
Differential diagnosis and management
Dr. Ipsita Mahapatra (PGT, Pediatrics)
Gauhati Medical College and Hospital

2. Definition – Acute Flaccid Paralysis
• Clinical syndrome characterised by rapid onset weakness.
• Weakness progresses to maximum within days to weeks.
• ‘Acute’ : Rapid progression from onset to maximum
• ‘Flaccid’ : Loss of muscle tone, ‘floppy’
Absence of spasticity or other upper motor neuron signs
• ‘Paralysis’ : Weakness, loss of voluntary movement
AFP is not a diagnosis but a broad clinical entity with an array of
diagnostic possibilities.

3. Case definition of Acute Flaccid Paralysis
In accordance with the Global Polio Eradication Initiative (1988), acute
flaccid paralysis is defined as :
• Any case of AFP in a child aged < 15 years for which no obvious cause
is found, Or
• Any case of paralytic illness in a person of any age when polio is
suspected.
Any case meeting this definition undergoes a thorough investigation to
determine if the paralysis is caused by polio.

5. Etiologies of AFP
(As per neuro-anatomical localisation)
1. SPINAL CORD
2. ANTERIOR HORN CELL DISORDERS
• Acute Tranverse Myelitis
• Compressive myelopathy (abscess, tumor)
• Anterior spinal artery syndrome
• Trauma
• Poliomyelitis
• Non-polio Enteroviruses

6. 3. NEUROPATHIES
4. NEUROMUSCULAR
JUNCTION DISORDERS
• Guillain Barre Syndrome
• Traumatic neuritis
• Post diphtheric neuropathy
• Acute Intermittent Porphyria
• Tick bite paralysis, Lyme disease
• CMV radiculopathy (in Immunocompromised
state)
• Heavy metal/Organophosphorous poisoning
• Myathenia gravis
• Neuroenvenomation (Snake bite)
• Botulism
• Lambert-Eaton syndrome

7. 5. MUSCLE
• Inflammatory myopathies
• Hypokalemic periodic Paralysis
• Hypermagnesemia
• Infections (viral myositis, trichinosis)

8. The 4 most common differential
diagnosis in a case of AFP are:
1. Poliomyelitis
2. Guillain Barre Syndrome
3. Acute Transverse Myelitis
4. Traumatic Neuritis

9. 1. Poliomyelitis
 Both the wild polio virus and the vaccine associated polio virus cause
anterior horn cell affliction to result in flaccid paralysis.
 Children under 5 y are the most frequently affected.
 Symptoms: The initial symptoms of polio are non-specific and include
fever, headache, vomiting, constipation, neck stiffness and pain in
limbs. The paralysis follows or accompanies these symptoms. The
maximal weakness evolves quickly over 1–2 d

10.  Clinical charateristics:
1. Fever at onset
2. Rapid progression of paralysis within 24–48 h
3. Asymmetric, proximal > distal muscles.
4. Preservation of sensory function often with
severe myalgias
5. Residual paralysis at 60 days
 Most of the children with paralytic polio die from
complications of bulbar paralysis and respiratory
failure.
 Management: mainly focused on meticulous
supportive care.

11. 2. Guillain-Barre Syndrome
 With the control of polio, GBS is the most
common cause of AFP in children.
 Worldwide its incidence is 0.6–4 cases per
100,000 per year.
 It most commonly occurs after an infection
triggered immune mediated attack on the nerve
axons or myelin.
 Antecedant respiratory or gastrointestinal
illnesses are commonly found in the history.

12. • GBS Subtypes:
1. Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
2. Acute Motor Axonal Neuropathy (AMAN)
3. Acute Motor Sensory Axonal Neuropathy (AMSAN)
4. Miller-Fischer Syndrome (MFS)
• Most common : AIDP > AMAN but AMAN maybe equally common in
Indian children.
• Clinical features: Initially pain, paraesthesia, or weakness in the
limbs which spreads proximally (ascending paralysis).
• Risk factors for children requiring ventilation are cranial nerve
involvement, increased CSF protein during first week of illness and
short period between antecedent illness and the onset of
symptoms.

13. • Investigations: nerve conduction studies and
lumbar puncture are done (to document CSF
albumin-cytological dissociation).
• When a child presents in the acute phase, the
differentiation from polio or enteroviral myelitis
can be done based on CSF. Viral myelitis would
show CSF pleocytosis, which would be
conspicuously absent in GBS.

15. 3. Transverse myelitis
• It is an acute demyelinating disorder of the spinal
cord which may occur alone or in combination with
demyelination in other portions of the nervous
system.
• Cause: Believed commonly that a previous infection
or immunization triggers transverse myelitis.
• Clinical characteristics:
Acute phase of spinal shock
Flaccid paraparesis or quadriparesis, urinary retention
or incontinence, absent reflexes and mute plantars,
sensory loss/level is frequently present.
After a few weeks
The signs of UMN dysfunction appear, in the form of
spasticity, and hypereflexia.

16. Early and Late stages of Transverse myelitis
Features Early stage Late Stage
Type of Paralysis LMN type, Flaccid UMN type, Spastic
Tone Decreased Increased
DTRs Areflexia Hyperreflexia
Babinski sign Absent Positive

17. • Suspect in any child with rapid onset flaccid
quadriparesis, early or persistent bladder or
bowel involvement, sensory loss or sensory level
on examination, with suggestion of UMN signs
on examination (e.g., up going plantars).
Respiratory failure may occur in higher level
lesions
• Urgent spinal MRI is needed to establish the
diagnosis.

18. 4. Traumatic neuritis (following injection)
• Traumatic neuritis is suspected in cases in which there is one limb
involvement.
• Definite history of injection in that limb (usually less than 24 h) before
the onset of paralysis.
• Associated with pain and hypothermia of affected limbs.
• It is sometimes difficult to distinguish it from polio. However, sensory
deficits and lack of CSF pleocytosis favour the diagnosis of traumatic
neuritis.
• Residual sensory deficits strongly favour the diagnosis of injection
neuritis.

19. Lesion
UMN
Spinal
Cord
LMN
Anterior Horn Cell
Radicle/Nerve root
Neuro muscular junction
Muscle

20. Diagnostic approach to a case of AFP
Information from history and a focussed neurological examination
looking at onset/pattern/progression of weakness, tone, deep tendon
reflexes, sensory examination, bowel and/or bladder involvement,
fever at onset of paralysis and etiology specific features.
1. Is the weakness due to a neurological cause? Rule out
pseudoparalysis
2. If neurological, is it an UMN or LMN lesion?
3. If LMN lesion, what is the level of lesion?
4. Likely etiology

21. Pseudoparalysis
• Apparent paralysis due to voluntary inhibition of motion because of
limb pain or incoordination but without actual paralysis.
• Orthopedic complaint
• Causes:
Trauma, fracture, sprain, arthritis/arthalgia, joint or periosteal bleeds,
joint or periarticular infections, abscess or inflammation

22. Localising the site of lesion
Important points in history taking – Clues to Diagnosis
Features Likely diagnosis
Fever at the onset of illness Polio
Loose stools/Cough 2-3 weeks prior GBS
Trauma/ IM injection Traumatic neuritis
Patch over tonsillar area, bull neck Diphtheria
Exposure to chemicals Arsenic, Lead poisoning
Abdominal Pain Porphyria, Lead poisoning

23. Features Likely diagnosis
Ptosis, blurred vision, respiratory
paralysis
Snake bite, Botulism, GBS (Miller
Fischer Variant)
Recurrent flaccid paralysis Periodic paralysis - Channelopathies
Dermatological manifestations:
Edema, Gottron’s papules
Inflammatory myopathy
(Dermatomyositis)
Headache, seizure, vomiting, altered
sensorium
Porphyria (associated
encephalopathy)
Ingestion of honey, canned food Botulism

24. Localising the site of lesion based on clinical signs
Important points in examination
Anatomical Level Clinical Signs
Brain stem Altered consciousness, Cranial nerve paralysis, UMN signs
Spinal Cord Bladder involvement, Sensory level, UMN signs (Below the
level of lesion), Plantars extensor
Anterior Horn Cell LMN type weakness, areflexia
Nerve root LMN type weakness, areflexia,
Peripheral nerve Sensory loss, glove and stocking sensory involvement
Neuromuscular
Junction
Diurnal variation, Fluctuating weakness
Muscle LMN weakness but reflexes preserved

25. Characteristics of common DDs of AFP
Feature Poliomyelitis GBS Transverse myelitis Traumatic neuritis
(following
injection)
Development of
paralysis
24-48hrs from
onset to full
paralysis
From hours to 4
weeks
From hours to 4
days
From hours to 4
days
Fever at onset of
weakness
High, always
present at onset
Uncommon May be present Present, if
underlying infection
being treated with
IM injection
Paralysis Asymmetric
Proximal > distal
Symmetric, mostly
ascending
Symmetric Affects only one
limb
Progression of
paralysis
Descending Ascending

26. Feature Poliomyelitis GBS Transverse myelitis Traumatic neuritis
(following
injection)
Sensation Intact, may have
diffuse myalgia
Cramps, tingling,
hypoanaesthesia of
palms and soles
Imapired below
level of lesion
Maybe impaired in
the distribution of
the affected nerve
Cranial Nerve
involvement
Affected in bulbar
and bulbospinal
variant
Usually affected Absent Absent
Respiratory
insufficiency
May be present May be present May be present Absent
Autonomic signs
and symptoms
Rare In severe cases (BP
alteration,
sweating, blushing,
body temp
fluctuation)
Present Hypothermia in
affected limb

27. Feature Poliomyelitis GBS Transverse myelitis Traumatic neuritis
(following
injection)
CSF Mild elevation of
lymphocytes 10-
200/ml
Albumino-
cytological
dissociation
(<10cells/ml, never
>50 cells/ml)
Normal (or
pleocytosis)
Normal
Bladder
dysfunction
Rare Occasionally
(Transient)
Present – Early and
persistent
Never
NCV studies Abnormal: Anterior
horn cell disease
(Normal during first
2 weeks)
Abnormal : slowed
conduction,
decreased motor
amplitudes
Normal Abnormal: s/o
motor-sensory
axonal damage
Diagnostic test Stool viral detection Nerve conduction
studies
MRI spine Nerve conduction
studies,
Electromyography

28. Based on history and examination:
1. Flaccid paraparesis with sensory level (early bladder dysfunction) : Acute
transverse myelitis, compressive myelopathy
2. Flaccid, afebrile, symmetric para/quadriparesis (+/- bulbar and respiratory
involvement) with areflexia and minimal sensory loss (but often sensory
symptoms) : Acute neuropathy or polyradiculopathy (eg. GBS)
3. Flaccid, febrile, pure motor, asymmetric paralysis (no bladder
involvement) : Enteroviral, Polio or Vaccine associated Poliomyelitis

29. 4. Flaccid motor-sensory lower limb monoparesis after IM injection :
Injection neuritis
5. Ophthalmoplegia, ptosis, bulbar weakness with motor weakness :
Miller-Fischer variant of GBS, Botulism, Myasthenia gravis
6. Proximal muscle weakness, muscle tenderness without sensory
symptoms or signs with preserved reflexes: Viral myositis,
Inflammatory myopathy (eg: dermatomyositis)

30. Management
A child with AFP is a medical emergency!
1. Initial management (aimed at stabilisation, anticipating and
identifying potential complications)
2. Detailed history and focussed neurological examination
3. Investigations
4. Specific therapy

31. A. Initial Management
• Assess vitals
• Respiratory care : Detect and manage respiratory muscle weakness:
irritability, sweating, poor feeding, shallow resp. efforts, air hunger,
reduced SBC/chest expansion.
• Bulbar weakness detection and management: voice change, poor cry,
pooling of secretions, gurgling sounds, difficulty in swallowing or choking
on feeds
• Managing cardiovascular instability
• Rule out dyselectrolytemia and snake envenomation
• Rule out spinal cord pathology

32. B. Detailed history and focussed neurological exam
C. Investigations
The choice of the initial investigations would depend on the information gained
from history and examination.
1. Routine Blood counts, CRP, Electrolytes
2. MRI Spine: suspicion of spinal cord compression or transverse myelitis.
3. CSF examination: A raised CSF cell count would be seen in patients with
transverse myelitis, infective myelitis viz. polio or enteroviral myelitis. A raised
CSF protein with normal cell count (albuminocytological dissociation) suggests
Guillain Barre syndrome

33. 3. Nerve Conduction studies and Electro Myography (EMG): These studies confirm
the involvement of nerves and help in diagnosis of anterior horn cell diseases.
These are particularly helpful to confirm Guillain Barre syndrome.
4. Creatine Kinase: Raised levels of muscle enzyme creatine kinase reflects acute
muscle fibre injury and may point towards a muscle disease. In the setting of AFP
this may be seen in children with viral myositis or inflammatory myopathy
5. Biochemistry: Potassium, Magnesium, Phosphate
6. ECG : To look for hypokalemia
7. Urine analysis : Urine for porpho-bilinogens, toxins: arsenic, lead etc.

34. D. Specific therapy
Once the diagnosis is ascertained, the specific treatment must be initiated.
Guillain-Barre Syndrome
IVIG is the treatment of choice for GBS, given the availability, ease of
administration and the safety compared with plasmapheresis. It is given in the
dose of 2 g/kg spread over 2–5 d or 400mg/kg/day for 5 days.
Transverse myelitis
High dose pulse corticosteroids are the recommended form therapy.
Methylprednisolone is given in a dose of 10–30 mg/kg/d (max:1 g/d) for 5 d
followed by oral prednisolone 1–2 mg/kg/d for 2 weeks and then tapered
over subsequent 2–4 wk.

35. Traumatic neuritis
Management is entirely supportive
Hypokalemic paralysis
Correction of potassium levels rapidly reverses the paralysis in these
children.
Poliomyelitis
AFP reporting and stool collection mandatory
Most of the children with paralytic polio die from complications of
bulbar paralysis and respiratory failure.
Management is mainly focused on meticulous supportive care with
physiotherapy, ambulation and prevention of deformities.
Compressive myelopathy
Spinal immobilization, neurosurgical intervention, steroids.

36. AFP Surveillance

37. Surveillance : definition
Surveillance : Continuous scrutiny of all
aspects of occurrence and spread of
disease that are pertinent to effective
control.
• Includes :
1. Collection of data
2. Analysis of data
3. Interpretation of data
4. Distribution of relevant data so that
necessary action can be taken

38. Types of public health surveillance
Passive Surveillance
Data/reports are sent by
designated health facilities
or individuals on their own,
periodically as a routine.
Active surveillance
A designated official, usually external
to the health facility visits
periodically and seeks to collect data
from individuals,/registers/log
books/medical records at a facility to
ensure that no reports/data are
incomplete or missing.

39. Global Polio eradication initiative
• With the launch of the Global Polio Eradication Initiative (1988), the
incidence of poliomyelitis across the world has declined significantly
through active surveillance, strengthening childhood immunisation
using OPV, improvement in sanitation and conducting "mop up"
campaigns in areas where cases of polio have been identified.
• The objectives of GPEI were:
1. To interrupt wild poliovirus transmission
2. To mainstream global polio eradication initiative
3. To develop products for global OPV cessation phase
4. To achieve certification of global polio eradication

40. • The strategy for the eradication of polio rested on immunising
every at risk child until there was no one left for the disease to
transmit to and the disease would eventually die out.
Current status :
• Only 2 countries are endemic for Polio as of 2021 : Pakistan and
Afghanistan. Nigeria has reported no new cases since 2014. Africa
was declared polio free in 2020.
• Malawi declared an outbreak of WPV type 1 on 17 February 2022.
This is the first case of wild poliovirus in Africa in more than 5 years.

41. • India was removed from the list of polio endemic countries in January
2012 after completing a year without reporting any case of polio in
January, a major milestone in the history of polio eradication.
• India declared polio-free on 27 March 2014, 3 years after the last case
was reported in January 2011 in West Bengal.
• Globally, type 2 virus serotype was declared eradicated in 2015, and
type 3 on 24 October 2019.

42. Source: mohfw/pulsepolioimmunisation

43. • Under the Endgame Polio Strategy 2013-2018, India switched over to
bivalent OPV in April 2016 excluding the OPV 2 strain which is mainly
responsible for vaccine derived polio.
1. Detect and interrupt all poliovirus transmission
2. Strengthen immunization systems and withdraw OPV
3. Contain poliovirus and certify interrupt of transmission
4. Plan post-polio legacy.
• Meanwhile, inactivated polio vaccine (IPV) was introduced in 2016 with
two fractional intradermal doses at 6 and 14 weeks along with bivalent
OPV
• Endgame Polio Strategy 2019-2023 is the current strategy by the GPEI.
• The ultimate aim is to stop the use of the oral polio vaccines altogether

44. Goals of Polio Endgame strategy 2019 - 2023

45. AFP surveillance is the strategy to screen for circulating wild polio virus
in the post-polio eradication phase.
1. Reporting of children with AFP
2. Transport and analysis of stool sample
3. Identify poliovirus in laboratory
4. Determine virus strain and origin

46. Case definition of Acute Flaccid Paralysis
In accordance with the Global Polio Eradication Initiative (1988), acute
flaccid paralysis is defined as :
• Any case of AFP in a child aged < 15 years for which no obvious cause
is found, Or
• Any case of paralytic illness in a person of any age when polio is
suspected.
Any case meeting this definition undergoes a thorough investigation to
determine if the paralysis is caused by polio.

47. • Every case of AFP <15 years must be reported.
• Within 48 hours of notification, a trained medical officer investigates
the case, proceeds with transportation of stool samples, outbreak
response immunizations (ORI) done in the affected community.
• A 60 day follow up examination of the case should also be done to
detect presence/absence of residual paralysis.

48. Purpose of AFP surveillance
• Helps to detect reliably areas where poliovirus transmission is
occurring.
• Thus, helps to identify areas of priority for focusing immunization
activities.
• It is the most reliable tool to measure the quality and impact of polio
immunization activities.
• For polio free certification, it is essential to provide evidence of the
absence of wild poliovirus transmission through a functioning and
sensitive surveillance system for at least 3 years after attaining a zero
polio case status.

49. Collecting stool specimen
Adequate stool:
• 2 stool specimen from every AFP case atleast 24 hours apart.
• Stool sample must be collected within 14 days of onset of paralysis to
maximise the chance of isolating poliovirus. Can be collected upto 60
days.
• Amount: About the size of one adult thumb (8 grams).
• Transport: The specimen should arrive at a WHO-accredited
laboratory within 72 hours of dispatch in good condition (i.e. no
dessication, no leakage, shipped on ice or frozen packs with adequate
documentation and evidence that the reverse cold chain was
maintained (2 to 8 degree celsius).

50. Sensitivity of AFP surveillance
Source : WHO best practices in active surveillance of polio eradication
2 Indicators set the gold standard for AFP surveillance quality:
1. At least 1 case of non-polio AFP reported yearly per 1,00,000 children
aged under 15 years (background rate of AFP) according to National
Polio Surveillance Project.
2. At least 80% of AFP cases should have 2 adequate stool samples.

52. References
• Ghai Essential Pediatrics 9th ed.
• WHO best practices in active surveillance of polio eradication
• PG textbook of Pediatrics, vol 3, Dr. Piyush Gupta
• Nelsons textbook of pediatrics
• Singhi SC, Sankhyan N, Shah R, Singhi P. Approach to a child
with acute flaccid paralysis. Indian J Pediatr. 2012 Oct

53. Thank You